Chapter 189 Menorrhagia
Diagnostic Summary
• Excessive menstrual bleeding—blood loss greater than 80 mL—occurring at regular cyclic intervals (cycles are usually but not necessarily of normal length).
• May be due to dysfunctional uterine bleeding (no organic cause); often due to local lesions (e.g., uterine myomas [fibroids], endometrial polyps, endometrial hyperplasia, endometrial cancer, adenomyosis, and endometritis); other causes are bleeding disorders and hypothyroid.
General Considerations
Etiology
As with any disease, proper determination of the cause is essential for effective treatment. The appropriate methodology for ruling out pathologic causes is beyond the scope of this chapter and can be found in any good text on gynecology (Table 189-1).1 It is important to be aware of the scope of causes so that one does not just assume that the problem is “dysfunctional uterine bleeding” (DUB)—defined as abnormal uterine bleeding without any demonstrable organic cause. Abnormal bleeding can include menorrhagia, oligomenenorrhea, polymenorrhea, metrorrhagia, menometrorrhagia, and intermenstrual bleeding. Abnormal bleeding is best understood by thinking in categories of abnormalities: hormonal, mechanical, and clotting. Hormonal causes include anovulation and luteal phase defects and stress, exogenous hormones, hypothyroidism, and ovarian cysts. Mechanical causes include uterine polyps, uterine fibroids, endometrial hyperplasia, uterine cancer, intrauterine devices (IUDs), atopic pregnancy, pregnancy, endometriosis, and endometritis. Clotting abnormalities include vitamin K deficiency, drug-induced hemorrhage (heparin, warfarin, aspirin), dysproteinemias, disseminated intravascular coagulation, severe hepatic disease, primary fibrinolysis, and circulating inhibitors of coagulation; not all of these will cause menorrhagia; rather, they give rise to other abnormal bleeding patterns.
TABLE 189-1 Pathologic Causes of Menorrhagia
| CAUSE | POSSIBLE ETIOLOGY |
|---|---|
| Anovulation | Excessive estrogen |
| Failure of midcycle surge of luteinizing hormone | |
| Hypothyroidism | |
| Hyperprolactinemia | |
| Polycystic ovary disease | |
| Intrauterine structural defects | Fibroids |
| Polyps | |
| Cancer | |
| Ectopic pregnancy | |
| Intrauterine devices | |
| Bleeding disorders | See Table 189-2 |
Data from Federman DD. Ovary. In Dale DC, Federman DD. Scientific American medicine. New York: Scientific American, 1997, 3:III:9-3:III:10.
Abnormalities in Prostaglandin Metabolism
The etiology of functional menorrhagia is currently believed to involve abnormalities in the biochemical processes of the endometrium that control the supply of arachidonic acid for prostaglandin synthesis.2,3 Menorrhagic endometrium incorporates arachidonic acid into neutral lipids to a much greater extent than normal, whereas its incorporation into phospholipids is lower. The greater arachidonic acid release during menstruation results in the higher production of series 2 prostaglandins, which are thought to be the major factor both in the excessive bleeding seen at menstruation and in the symptoms of dysmenorrhea. The excessive bleeding during the first 3 days appears to be due to the vasodilatory properties of prostaglandins (PGs) E2 and PGI2 and the antiaggregating activity of PGI2, whereas the pain of dysmenorrhea is due to the overproduction of PGF2a.
Thyroid Abnormalities
The association of overt hypothyroidism or hyperthyroidism with menstrual disturbances is well known. However, even minimal thyroid dysfunction, particularly minimal subclinical insufficiency as determined by testing the thyroid stimulating hormone (TSH), may be responsible for menorrhagia and other menstrual disturbances.4 Patients with minimal thyroid insufficiency and menorrhagia have shown dramatic responses to thyroxine.4 It has been recommended that patients with long-standing menstrual dysfunction (who have no obvious uterine disease) should be considered for TSH testing. This approach is preferable to the empiric use of thyroid hormone.
Estimating Menstrual Blood Loss
Physicians often believe that they can assess menstrual blood loss by asking the patient to estimate the number of pads or tampons used during each period and the duration of the period. However, studies have demonstrated that there is no correlation between measured blood loss and these assessments.1,5,6 A woman’s assessment of her blood loss is extremely subjective, as demonstrated by one study finding that 40% of women with a menstrual blood loss exceeding 80 mL considered their periods only moderately heavy or scanty, whereas 14% of those with a measured loss of less than 20 mL judged their periods to be heavy.6
Therapeutic Considerations
Nutrition
Iron Deficiency
A menstrual blood loss exceeding 60 mL per period is associated with negative iron balance in most cases.7 Although menstrual blood loss is well recognized as a major cause of iron-deficiency anemia in fertile women, it is not as well known that chronic iron deficiency can be a cause of menorrhagia. Taymor et al8 have made such a suggestion on the basis of several observations:
• Response to iron supplementation alone in 74 of 83 patients (in whom organic disease had been excluded)
• High rate of organic disease (fibroids, polyps, adenomyosis, etc.) in the patients with no response to iron supplementation
• Associated rise in serum iron levels in 44 of 57 patients
• Decreased response to iron therapy when initial serum iron levels were high
• Correlation of menorrhagia with depleted tissue iron stores (bone marrow) irrespective of serum iron level
• A significant double-blind placebo-controlled study displaying improvement in 75% of those given iron supplementation compared with 32.5% of those given the placebo
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